Considerable progress has been made in the last 20 years in identifying the complex biochemical events that occur at the synapse during synaptic transmisssion. Considerably less is known, however, of the specific biochemical synaptic events that most probably initiate and maintain a seizure focus. The proposed experiments are designed to apply recent experimental advances in our understanding of synaptic function to this question. Specifically, the following proposal is designed to examine changes in phosphoprotein metabolism in synaptic membranes isolated from rats that have undergone the "Kindling" procedure, an experimental model of epilepsy. Phosphoprotein metabolism is of interest because recent evidence indicates a critical role for phosphorylated proteins in the regulation of synaptic function, and converging lines of evidence now indicate the possibility that they also have an involvement in the etiology of epilepsy. The "Kindling" model of epilepsy is used because the behavioral and pharmacological properties of kindling make it a particularly attractive experimental model. Experiment 1 will use the (14C)-2-deoxy-D-glucose technique to map the spread of seizure activity from a kindled seizure focus in the amygdala. This information will be useful in determining the brain regions, in addition to the amygdala, to be examined in Experiment 2. In Experiment 2 synaptic membranes from amygdala kindled rats will be isolated, and membrane phosphoproteins will be radioactively labeled with 32P, separated by gel electrophoresis, and located by autoradiography. It is predicted that specific classes of synaptic membrane phosphoproteins will show altered phosphate metabolism following the kindling procedure. This information will advance our understanding of the synaptic events underlying kindling, and by analogy, epilepsy.